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Article type: Research Article
Authors: Weill, D. | Setiadi, H. | Wautier, M.P. | Guillausseau, P.J. | Liote, F. | Wautier, J.L.;
Affiliations: I.V.S., INSERM U150, Hôpital Lariboisière, Paris, France | Department of Internal Medicine, Hôpital Lariboisière, Paris, France
Note: [] Correspondence to J.L.Wautier. Immunohematologie, Hôpital Lariboisière, 2 rue Ambroise Paré, Paris 75010, France.
Abstract: Leukocyte adhesion to endothelium is an important phenomenon in inflammatory conditions and vascular diseases. Monocyte adhesion involved leukocyte adhesion molecules such as the CD11b/CDl8 complex. We have studied the effect of pentoxifylline on the adhesion of monocyte from normal subjects and diabetic patients to human endothelial cells (HEC) in culture and on the expression of CD11b/CDl8 complex on monocytes. Monocyte adhesion was potentiated when HEC were stimulated by interleukin-1β (1L-1β). Pentoxifylline decreased the adhesion of monocytes to unstimulated or 1L-1β stimulated HEC at concentration of 1μM and 5mM respectively. Pentoxifylline has a higher inhibitory effect than hydrocortisone at 0.1mM concentration, but in association the two drugs had an additive effect. Pentoxifylline at concentrations ranging between 0.1mM and 5mM significantly inhibited CD11b/CD18 expression both in normal subjects and diabetic patients. Pentoxifylline appeared to alter monocyte adhesive properties.
Keywords: Leukocyte Adhesion Molecule, diabetes mellitus, Pentoxifylline
DOI: 10.3233/CH-1992-12509
Journal: Clinical Hemorheology and Microcirculation, vol. 12, no. 5, pp. 713-724, 1992
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